The four serotypes of dengue recognize the same putative receptors in Aedes aegypti midgut and Ae. albopictus cells

Mercado-Curiel, Ricardo F.; Esquinca-Avilés, Héctor Armando; Tovar, Rosalinda; Diaz-Badillo, Alvaro; Camacho-Nuez, Minerva; Muñoz, Marı́a de Lourdes

doi:10.1186/1471-2180-6-85

Cited by 54 publications

(25 citation statements)

References 47 publications

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“…Antibodies against an 80 kDa protein in C6/36 cells [ 80 ] and antibodies against 67 and 80 kDa proteins, located at the apical membrane of the midgut epithelium in Ae. aegypti , inhibited DENV1-4 infection [ 81 ]. In another study, utilizing three different Ae.…”

Section: The Midgut Infection Barriermentioning

confidence: 99%

Tissue Barriers to Arbovirus Infection in Mosquitoes

Franz

Kantor

Passarelli

et al. 2015

Viruses

379

393

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Arthropod-borne viruses (arboviruses) circulate in nature between arthropod vectors and vertebrate hosts. Arboviruses often cause devastating diseases in vertebrate hosts, but they typically do not cause significant pathology in their arthropod vectors. Following oral acquisition of a viremic bloodmeal from a vertebrate host, the arbovirus disease cycle requires replication in the cellular environment of the arthropod vector. Once the vector has become systemically and persistently infected, the vector is able to transmit the virus to an uninfected vertebrate host. In order to systemically infect the vector, the virus must cope with innate immune responses and overcome several tissue barriers associated with the midgut and the salivary glands. In this review we describe, in detail, the typical arbovirus infection route in competent mosquito vectors. Based on what is known from the literature, we explain the nature of the tissue barriers that arboviruses are confronted with in a mosquito vector and how arboviruses might surmount these barriers. We also point out controversial findings to highlight particular areas that are not well understood and require further research efforts.

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Section: The Midgut Infection Barriermentioning

confidence: 99%

Tissue Barriers to Arbovirus Infection in Mosquitoes

Franz

Kantor

Passarelli

et al. 2015

Viruses

379

393

View full text Add to dashboard Cite

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“…aegypti susceptibility to infection with DENV. Genes that have also been shown to play a role in mosquito competence include genes producing proteins that bind with an arbovirus [104,105,106,107,108,109,110,111,112,113]. A variety of Ae.…”

Section: Mosquito Genetic Factors Influence Mosquito Competence Fomentioning

confidence: 99%

Nature, Nurture and Evolution of Intra-Species Variation in Mosquito Arbovirus Transmission Competence

Tabachnick

2013

IJERPH

105

111

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Mosquitoes vary in their competence or ability to transmit arthropod-borne viruses (arboviruses). Many arboviruses cause disease in humans and animals. Identifying the environmental and genetic causes of variation in mosquito competence for arboviruses is one of the great challenges in public health. Progress identifying genetic (nature) and environmental (nurture) factors influencing mosquito competence for arboviruses is reviewed. There is great complexity in the various traits that comprise mosquito competence. The complex interactions between environmental and genetic factors controlling these traits and the factors shaping variation in Nature are largely unknown. The norms of reaction of specific genes influencing competence, their distributions in natural populations and the effects of genetic polymorphism on phenotypic variation need to be determined. Mechanisms influencing competence are not likely due to natural selection because of the direct effects of the arbovirus on mosquito fitness. More likely the traits for mosquito competence for arboviruses are the effects of adaptations for other functions of these competence mechanisms. Determining these other functions is essential to understand the evolution and distributions of competence for arboviruses. This information is needed to assess risk from mosquito-borne disease, predict new mosquito-arbovirus systems, and provide novel strategies to mitigate mosquito-borne arbovirus transmission.

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“…FLVs enter host cells through a receptor-mediated mechanism [35]. Multiple host cell receptors have been identified to facilitate FLV entry, including GAG [6,36], heat-shock proteins (heat-shock protein 70, 90, R67, R80) [15,25,37], a 45 kD mosquito glycoprotein [38], neolactotertraosylceramide [16], CD14 [17], GRP78/BiP [18], phosphatidylserine (PS) receptors such as T-cell immunoglobulin and mucin domain receptor (TIM) [39], Tyrosine-protein kinase receptor (TYRO3) [40], and AXL [41], and proto-oncogene tyrosine-protein kinase (MERTK) [42]. C-type lectins implicated in FLV entry include DC-SIGN [22,43], and the mannose receptor [23], C-type lectin domain family 5 member A (CLEC5A) [44].…”

Section: Glycan-mediated Flavivirus Entrymentioning

confidence: 99%

“…GAGs are involved in many biological processes, including cell adhesion, cell migration, tissue repair, ECM assembly, inflammation, and pathogenesis [14]. After successfully making contact with the host cell surface through their binding to GAGs, FLV next interact with protein-based receptors [15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32]. Finally, FLVs infiltrate into the host cell through clathrin-mediated endocytosis, accompanied by a conformation change of envelope protein and membrane fusion and release of the viral genome (Figure 2) [33,34].…”

Section: Introductionmentioning

confidence: 99%

Pathogenesis and Inhibition of Flaviviruses from a Carbohydrate Perspective

Kim

Linhardt

2017

Pharmaceuticals

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Flaviviruses are enveloped, positive single stranded ribonucleic acid (RNA) viruses with various routes of transmission. While the type and severity of symptoms caused by pathogenic flaviviruses vary from hemorrhagic fever to fetal abnormalities, their general mechanism of host cell entry is similar. All pathogenic flaviviruses, such as dengue virus, yellow fever virus, West Nile virus, Japanese encephalitis virus, and Zika virus, bind to glycosaminglycans (GAGs) through the putative GAG binding sites within their envelope proteins to gain access to the surface of host cells. GAGs are long, linear, anionic polysaccharides with a repeating disaccharide unit and are involved in many biological processes, such as cellular signaling, cell adhesion, and pathogenesis. Flavivirus envelope proteins are N-glycosylated surface proteins, which interact with C-type lectins, dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) through their glycans. In this review, we discuss both host and viral surface receptors that have the carbohydrate components, focusing on the surface interactions in the early stage of flavivirus entry. GAG-flavivirus envelope protein interactions as well as interactions between flavivirus envelope proteins and DC-SIGN are discussed in detail. This review also examines natural and synthetic inhibitors of flaviviruses that are carbohydrate-based or carbohydrate-targeting. Both advantages and drawbacks of these inhibitors are explored, as are potential strategies to improve their efficacy to ultimately help eradicate flavivirus infections.

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The four serotypes of dengue recognize the same putative receptors in Aedes aegypti midgut and Ae. albopictus cells

Cited by 54 publications

References 47 publications

Tissue Barriers to Arbovirus Infection in Mosquitoes

Tissue Barriers to Arbovirus Infection in Mosquitoes

Nature, Nurture and Evolution of Intra-Species Variation in Mosquito Arbovirus Transmission Competence

Pathogenesis and Inhibition of Flaviviruses from a Carbohydrate Perspective

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